C23. Age particularity of mitochondrial respiration and lipid peroxidation processes in rats under NO-system activation

Nitric Oxide ◽  
2007 ◽  
Vol 17 ◽  
pp. 25
Author(s):  
K. Murashchuk ◽  
O. Ikkert
Keyword(s):  
Lipid Peroxidation ◽  
Mitochondrial Respiration ◽  
System Activation ◽  
Peroxidation Processes

scholarly journals miR-21-5p regulates mitochondrial respiration and lipid content in H9C2 cells

2019 ◽  
Vol 316 (3) ◽  
pp. H710-H721 ◽  
Author(s):  
Victoria L. Nasci ◽  
Sandra Chuppa ◽  
Lindsey Griswold ◽  
Kathryn A. Goodreau ◽  
Ranjan K. Dash ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acid ◽  
Palmitic Acid ◽  
Fatty Acid Oxidation ◽  
Lipid Content ◽  
Mitochondrial Respiration ◽  
Acid Oxidation ◽  
H9c2 Cells ◽  
Cellular Lipid ◽  
Transfected Cells

Cardiovascular-related pathologies are the single leading cause of death in patients with chronic kidney disease (CKD). Previously, we found that a 5/6th nephrectomy model of CKD leads to an upregulation of miR-21-5p in the left ventricle, targeting peroxisome proliferator-activated receptor-α and altering the expression of numerous transcripts involved with fatty acid oxidation and glycolysis. In the present study, we evaluated the potential for knockdown or overexpression of miR-21-5p to regulate lipid content, lipid peroxidation, and mitochondrial respiration in H9C2 cells. Cells were transfected with anti-miR-21-5p (40 nM), pre-miR-21-5p (20 nM), or the appropriate scrambled oligonucleotide controls before lipid treatment in culture or as part of the Agilent Seahorse XF fatty acid oxidation assay. Overexpression of miR-21-5p attenuated the lipid-induced increase in cellular lipid content, whereas suppression of miR-21-5p augmented it. The abundance of malondialdehyde, a product of lipid peroxidation, was significantly increased with lipid treatment in control cells but attenuated in pre-miR-21-5p-transfected cells. This suggests that miR-21-5p reduces oxidative stress. The cellular oxygen consumption rate (OCR) was increased in both pre-miR-21-5p- and anti-miR-21-5p-transfected cells. Levels of intracellular ATP were significantly higher in anti-mR-21-5p-transfected cells. Pre-miR-21-5p blocked additional increases in OCR in response to etomoxir and palmitic acid. Conversely, anti-miR-21-5p-transfected cells exhibited reduced OCR with both etomoxir and palmitic acid, and the glycolytic capacity was concomitantly reduced. Together, these results indicate that overexpression of miR-21-5p attenuates both lipid content and lipid peroxidation in H9C2 cells. This likely occurs by reducing cellular lipid uptake and utilization, shifting cellular metabolism toward reliance on the glycolytic pathway. NEW & NOTEWORTHY Both overexpression and suppression of miR-21-5p augment basal and maximal mitochondrial respiration. Our data suggest that reliance on glycolytic and fatty acid oxidation pathways can be modulated by the abundance of miR-21-5p within the cell. miR-21-5p regulation of mitochondrial respiration can be modulated by extracellular lipids.

P147 Lipid peroxidation processes in newborns born from mothers who consumed alcohol during pregnancy

2017 ◽  
Author(s):  
Lyubov Rychkova ◽  
Anait Marianian ◽  
Marina Darenskaya ◽  
Lyudmila Grebenkina ◽  
Barbara Bonner ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Peroxidation Processes

scholarly journals Effect of alimentary synthetic estrogen on cell compensatory mechanisms in rats of different ages

Biologija ◽  
2017 ◽  
Vol 63 (2) ◽  
Author(s):  
Oleh Yermishev ◽  
Tatyana Lykholat ◽  
Olena Lykholat
Keyword(s):  
Lipid Peroxidation ◽  
Female Rats ◽  
Compensatory Mechanisms ◽  
Neurotransmitter System ◽  
Enzyme Systems ◽  
Synthetic Estrogen ◽  
System Components ◽  
Different Ages ◽  
Peroxidation Processes ◽  
Cholinergic Neurotransmitter

Results of a study of lipid peroxidation, antioxidant system components, and cholinergic neurotransmitter system in the organs of experimental rats of different ages exposed to alimentary synthetic estrogen are presented. Given the state of peroxidation processes and AChE activities in female rats exposed to xenoestrogen, it is possible to assume the possibility of the restructuring of the functioning of mediator and enzyme systems and additional strengthening of pathological symptoms. In the future, such phenomena may trigger the reduction of potential of compensatory mechanisms in compromising the health of the consumers. In puberty, females were more sensitive to nutritional synthetic estrogen than mature animals, thus proving that age is another factor in xenoestrogen exposure. Because of the changes in the rates of reactions to detoxification but not to the metabolism of estrogen received into the organism, particularly with food, with age the animals were less susceptible to the effects of these substances.

scholarly journals Lipid peroxidation during chronic inflammation

2018 ◽  
Vol 6 (2) ◽  
pp. 38-53
Author(s):  
Irina Sokolovskaya ◽  
Valentina Nechiporenko ◽  
Natalia Gordiyenko ◽  
Olena Pozdnyakova ◽  
Svitlana Volkova ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Inflammatory Process ◽  
Positive Influence ◽  
Biologically Active ◽  
Peroxide Oxidation ◽  
Normal Functioning ◽  
Peroxidation Processes ◽  
Energy Processes ◽  
Active Substances ◽  
Physiological Systems

To keep needed level of peroxide lipid oxidation is necessary for the normal functioning of physiological systems. It is supported by the balance of anti-and prooxidant systems. The positive influence of lipid peroxidation processes in the organism is manifested by the restoration of the composition and maintenance of the properties of biological membranes, participation in energy processes, cell division, synthesis of biologically active substances. It has been established that the inflammatory process is accompanied by changes in lipid metabolism and the intensity of peroxide oxidation.

Superoxide anion generation and lipid peroxidation processes during hemodialysis with reused cuprophan dialyzers

1990 ◽  
Vol 8 (5) ◽  
pp. 429-432 ◽  
Author(s):  
K TRZNADEL ◽  
M LUCIAK ◽  
L PAWLICKI ◽  
J KEDZIORA ◽  
J BLASZCZYK ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Anion ◽  
Superoxide Anion Generation ◽  
Peroxidation Processes

Lipid peroxidation processes in organism during crush syndrome

1998 ◽  
Vol 5 ◽  
pp. 72
Author(s):  
R.R. Rukhadze ◽  
N. Pavliashvili ◽  
V.A. Kipiani
Keyword(s):  
Lipid Peroxidation ◽  
Crush Syndrome ◽  
Peroxidation Processes

scholarly journals Dynasore Blocks Ferroptosis through Combined Modulation of Iron Uptake and Inhibition of Mitochondrial Respiration

Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2259
Author(s):  
Laura Prieto Clemente ◽  
Malena Rabenau ◽  
Stephan Tang ◽  
Josefina Stanka ◽  
Eileen Cors ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Mitochondrial Respiration ◽  
Iron Uptake ◽  
Neuronal Cell ◽  
Protective Effects ◽  
Ros Scavenging ◽  
Intact Cells ◽  
Active Inhibitor ◽  
Cord Injury

Ferroptosis is a form of regulated necrosis characterized by a chain-reaction of detrimental membrane lipid peroxidation following collapse of glutathione peroxidase 4 (Gpx4) activity. This lipid peroxidation is catalyzed by labile ferric iron. Therefore, iron import mediated via transferrin receptors and both, enzymatic and non-enzymatic iron-dependent radical formation are crucial prerequisites for the execution of ferroptosis. Intriguingly, the dynamin inhibitor dynasore, which has been shown to block transferrin receptor endocytosis, can protect from ischemia/reperfusion injury as well as neuronal cell death following spinal cord injury. Yet, it is unknown how dynasore exerts these cell death-protective effects. Using small interfering RNA suppression, lipid reactive oxygen species (ROS), iron tracers and bona fide inducers of ferroptosis, we find that dynasore treatment in lung adenocarcinoma and neuronal cell lines strongly protects these from ferroptosis. Surprisingly, while the dynasore targets dynamin 1 and 2 promote extracellular iron uptake, their silencing was not sufficient to block ferroptosis suggesting that this route of extracellular iron uptake is dispensable for acute induction of ferroptosis and dynasore must have an additional off-target activity mediating full ferroptosis protection. Instead, in intact cells, dynasore inhibited mitochondrial respiration and thereby mitochondrial ROS production which can feed into detrimental lipid peroxidation and ferroptotic cell death in the presence of labile iron. In addition, in cell free systems, dynasore showed radical scavenger properties and acted as a broadly active antioxidant which is superior to N-acetylcysteine (NAC) in blocking ferroptosis. Thus, dynasore can function as a highly active inhibitor of ROS-driven types of cell death via combined modulation of the iron pool and inhibition of general ROS by simultaneously blocking two routes required for ROS and lipid-ROS driven cell death, respectively. These data have important implications for the interpretation of studies observing tissue-protective effects of this dynamin inhibitor as well as raise awareness that off-target ROS scavenging activities of small molecules used to interrogate the ferroptosis pathway should be taken into consideration.

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